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Richards, F.

Publications and source records attributed to Richards, F..

3 recordsLinked to original sources

DroneMegaDetector, A Generalised Model For Detecting Large Mammals In Aerial Imagery

Large-scale drone surveys can generate imagery across substantial geographic areas, but automated analysis remains challenging because animal appearance, target density, imaging conditions and target scale can vary considerably between surveys. We present a general-purpose RF-DETR Medium object detector developed for large-scale aerial drone imagery and evaluate its ability to generalise across taxa, environments and survey conditions. Unlike specialist counting systems that primarily return point detections, the proposed detector produces explicit bounding boxes, providing a spatial representation that can support counting as well as downstream detection, classification and tracking workflows. We evaluated the detector on an internal held-out test set and independent external datasets spanning cattle, birds, caribou and hippopotamuses, together with imagery acquired under substantially different survey conditions. On the comparative Cattle dataset, RF-DETR matched OWL across the reported point-localisation and counting metrics, while on Caribou it achieved almost identical point-based detection performance and similar aggregate counting error. Performance varied across the broader external benchmark, with reduced transfer to unseen avian imagery and differences between models across datasets. At high altitude on SAVMAP, all evaluated approaches experienced substantial performance degradation, demonstrating a shared limitation associated with small target scale. Overall, the results show that a general-purpose detector trained on heterogeneous drone imagery can provide competitive localisation and counting performance across diverse datasets while retaining explicit bounding-box outputs. The trained model weights and inference code are provided online to support reproducible large-scale aerial wildlife monitoring and further development of drone-based computer-vision workflows.

ecology↗

Identification of RBPMS as a smooth muscle master splicing regulator via proximity of its gene with super-enhancers

Alternative splicing (AS) programs are primarily controlled by regulatory RNA binding proteins (RBPs). It has been proposed that a small number of master splicing regulators might control cell-specific splicing networks and that these RBPs could be identified by proximity of their genes to transcriptional super-enhancers. Using this approach we identified RBPMS as a critical splicing regulator in differentiated vascular smooth muscle cells (SMCs). RBPMS is highly down-regulated during phenotypic switching of SMCs from a contractile to a motile and proliferative phenotype and is responsible for 20% of the AS changes during this transition. RBPMS directly regulates AS of numerous components of the actin cytoskeleton and focal adhesion machineries whose activity is critical for SMC function in both phenotypes. RBPMS also regulates splicing of other splicing, post-transcriptional and transcription regulators including the key SMC transcription factor Myocardin, thereby matching many of the criteria of a master regulator of AS in SMCs.

molecular biology↗

Length of uninterrupted CAG repeats, independent of polyglutamine size, results in increased somatic instability and hastened age of onset in Huntington disease

Huntington disease (HD) is an autosomal dominant neurological disorder that is caused by a CAG repeat expansion, translated into polyglutamine, in the huntingtin (HTT) gene. Although the length of this repeat polymorphism is inversely correlated with age of onset (AOO), it does not fully explain the variability in AOO. Genomic studies have provided evidence for the involvement of DNA repair in modifying this trait, potentially through somatic repeat instability. We therefore assessed genetic variants within the 12bp interrupting sequence between the pathogenic CAG repeat and the polymorphic proline (CCG) tract in the HTT gene and identified variants that result in complete loss of interruption (LOI) between the adjacent CAG/CCG repeats. Analysis of multiple HD pedigrees showed that this variant is associated with dramatically earlier AOO and is particularly relevant to HD patients with reduced penetrance alleles. On average AOO of HD is hastened by an average of 25 years in LOI carriers. This finding indicates that the number of uninterrupted CAG repeats is the most significant contributor to AOO of HD and is more impactful than polyglutamine length, which is not altered in these patients. We show that the LOI variant is associated with increases in both somatic and germline repeat instability, demonstrating a potential mechanism for this effect. Screening individuals from the general population (n=2,674 alleles) suggests that the variant occurs only in expanded CAG repeat alleles. Identification of this modifier has important clinical implications for disease management of HD families, especially for those in the reduced penetrance ranges.

genetics↗